Research | Publications | Lab Members
Michael T. Berton, Ph.D.
Microbiology & Immunology
University of Texas Health Science Center San Antonio
4.037V - MEDTel: (210) 567-3931Fax: (210) 567-6428Email:
Dr. Berton has a broad background in cellular and lolecular immunology, molecular biology, and the study of infectious diseases. He also has extensive expertise in the areas of cytokine signaling and Toll-like receptor signaling. Dr. Berton completed his graduate and post-doctoral training in the laboratories of two National Academy of Sciences members, Dr. Robert G. Webster and Dr. Ellen S. Vitetta, where he made significant contributions to the feilds of influenza genetics and B cell heavy chain class switching, respectfully. Early in his independent career, Dr. Berton studied the regulation of immunoglobulin heavy chain gene exspression and class switching in B lymphocyctes. His lab made early contributions to understanding how IL-4-activated STAT6 and CD40L-CD40 interactions regulate germilne immunoglobulin heavy chain gene transcription and heavy chain class switching. In 2002, Dr. Berton began to also study Toll-likereceptor signaling during immune responses to infection. His lab has now developed important collaborative partners, published several papers in this area, and made exciting novel findings that are now poised to pursue.
Ph.D., University of Tennessee center for the Health Sciences, Memphis, TN
Keywords: Cytokine and Toll-like receptor signaling; immunity to infection; Francisella tularensis
Dr. Berton's laboratory is interested in the molecular and cell biology of host cell signaling pathways that regulate innate and adaptive immune responses, and in the mechanisms that pathogens use to manipulate and evade host immunity. They are currently studying the role of Toll-like receptor (TLR) signaling in the immune response to the intracellular bacterial pathogen, Francisella tularensis. F. tularensis is a Gram-negative, facultative, intracellular bacterial pathogen that causes the disease tularemia. F. tularensis type A and B strains have been classified as Tier 1 biodefense agents because of their high infectivity, extreme virulence, and ability to be disseminated by aerosol, yet there is no licensed vaccine for this highly virulent pathogen. A critical Francisella virulence trait is its ability to suppress the innate and adaptive immune responses, but little is known about the mechanisms underlying this suppression. The innate immune response to pathogens is initiated when the host is alerted to infection as a result of recognition of pathogen-derived molecules by pattern recognition receptors (PRRs), such as the Toll-like receptors (TLRs), that recognize and bind to conserved molecular motifs expressed by many pathogens. The TLRs are evolutionarily conserved, germline-encoded receptors that signal many cell types via a set of cytoplasmic signaling adaptors that lead to MAP kinase and NF-κB activation. Binding of TLRs to pathogen-derived molecules induces the expression of chemokines and pro-inflammatory cytokines by many different cell types, and upregulates the expression of MHC and co-stimulatory molecules on antigen-presenting cells required for the activation of T cells. Current studies in the lab are focused on identifying the role that TLR signaling plays in the host protective response against F. tularensis infection and on the mechanisms used by F. tularensis to evade or suppress those responses in a mouse model of pulmonary tularemia. Thier expectation is that these studies will identify critical immune signaling pathways and mechanisms of immune evasion that must be considered in the development of a safe and effective F. tularensis vaccine.
2004, Executive Research Committee Incentive Award, UTHSCSA
2012, Laboratory Travel Award from the American Association of Immunologists